南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2015年
4期
549-552
,共4页
李芳%曾欧%罗健%吴志雄%肖婷%张晶晶%杨军
李芳%曾歐%囉健%吳誌雄%肖婷%張晶晶%楊軍
리방%증구%라건%오지웅%초정%장정정%양군
硫化氢%糖尿病%心肌纤维化%Collagen I%MAPK1/3%MMP-8
硫化氫%糖尿病%心肌纖維化%Collagen I%MAPK1/3%MMP-8
류화경%당뇨병%심기섬유화%Collagen I%MAPK1/3%MMP-8
hydrogen sulfide%diabetes mellitus%myocardial fibrosis%collagen I%MAPK1/3%MMP-8
目的:探讨气体信号分子硫化氢(H2S)对糖尿病大鼠心肌纤维化及MAPK1/3和MMP-8蛋白表达的影响。方法40只SD大鼠随机分为4组:正常对照组、糖尿病大鼠组(STZ组)、硫化氢干预糖尿病大鼠组(STZ+H2S组)和硫化氢干预正常大鼠组(H2S组)。用腹腔注射链脲佐菌素(STZ)(40 mg/kg)建立糖尿病大鼠模型;对照组每天腹腔注射生理盐水;STZ+H2S组与H2S组每天腹腔注射硫氢化钠(H2S供体)溶液(100μmol/kg),8周后处死大鼠,HE染色观察心肌纤维病理形态学变化,Western blot法检测Collagen I、MAPK1/3和MMP-8蛋白的表达。结果与对照组相比,糖尿病组大鼠心肌组织胶原含量明显升高,心肌间质纤维化,Collagen I、MAPK1/3和MMP-8蛋白表达水平显著升高(P<0.05);糖尿病大鼠经硫化氢干预后大部分心肌纤维呈平行排列,结构清晰,间质有少量疏松结缔组织,Collagen I、MAPK1/3和MMP-8蛋白表达水平明显下调(P<0.05),而非糖尿病硫化氢干预组心肌纤维化程度及心肌组织Collagen I、MAPK1/3和MMP-8蛋白表达水平较对照组均无明显差异(P>0.05)。结论 H2S可改善糖尿病大鼠心肌纤维化,其机制可能与抑制MAPK1/3/MMP-8信号通路有关。
目的:探討氣體信號分子硫化氫(H2S)對糖尿病大鼠心肌纖維化及MAPK1/3和MMP-8蛋白錶達的影響。方法40隻SD大鼠隨機分為4組:正常對照組、糖尿病大鼠組(STZ組)、硫化氫榦預糖尿病大鼠組(STZ+H2S組)和硫化氫榦預正常大鼠組(H2S組)。用腹腔註射鏈脲佐菌素(STZ)(40 mg/kg)建立糖尿病大鼠模型;對照組每天腹腔註射生理鹽水;STZ+H2S組與H2S組每天腹腔註射硫氫化鈉(H2S供體)溶液(100μmol/kg),8週後處死大鼠,HE染色觀察心肌纖維病理形態學變化,Western blot法檢測Collagen I、MAPK1/3和MMP-8蛋白的錶達。結果與對照組相比,糖尿病組大鼠心肌組織膠原含量明顯升高,心肌間質纖維化,Collagen I、MAPK1/3和MMP-8蛋白錶達水平顯著升高(P<0.05);糖尿病大鼠經硫化氫榦預後大部分心肌纖維呈平行排列,結構清晰,間質有少量疏鬆結締組織,Collagen I、MAPK1/3和MMP-8蛋白錶達水平明顯下調(P<0.05),而非糖尿病硫化氫榦預組心肌纖維化程度及心肌組織Collagen I、MAPK1/3和MMP-8蛋白錶達水平較對照組均無明顯差異(P>0.05)。結論 H2S可改善糖尿病大鼠心肌纖維化,其機製可能與抑製MAPK1/3/MMP-8信號通路有關。
목적:탐토기체신호분자류화경(H2S)대당뇨병대서심기섬유화급MAPK1/3화MMP-8단백표체적영향。방법40지SD대서수궤분위4조:정상대조조、당뇨병대서조(STZ조)、류화경간예당뇨병대서조(STZ+H2S조)화류화경간예정상대서조(H2S조)。용복강주사련뇨좌균소(STZ)(40 mg/kg)건립당뇨병대서모형;대조조매천복강주사생리염수;STZ+H2S조여H2S조매천복강주사류경화납(H2S공체)용액(100μmol/kg),8주후처사대서,HE염색관찰심기섬유병리형태학변화,Western blot법검측Collagen I、MAPK1/3화MMP-8단백적표체。결과여대조조상비,당뇨병조대서심기조직효원함량명현승고,심기간질섬유화,Collagen I、MAPK1/3화MMP-8단백표체수평현저승고(P<0.05);당뇨병대서경류화경간예후대부분심기섬유정평행배렬,결구청석,간질유소량소송결체조직,Collagen I、MAPK1/3화MMP-8단백표체수평명현하조(P<0.05),이비당뇨병류화경간예조심기섬유화정도급심기조직Collagen I、MAPK1/3화MMP-8단백표체수평교대조조균무명현차이(P>0.05)。결론 H2S가개선당뇨병대서심기섬유화,기궤제가능여억제MAPK1/3/MMP-8신호통로유관。
Objective To explore the effects of hydrogen sulfide (H2S) on myocardial fibrosis and expressions of MAPK1/3 and MMP-8 in diabetic rats. Methods Forty adult male SD rats were randomized into 4 groups, namely the control group, diabetes mellitus group (STZ group), diabetes mellitus with H2S treatment group (STZ+H2S group), and normal rats with H2S treatment group (H2S group). Diabetes was induced by intraperitoneal injections of 40 mg/kg streptozotocin (STZ). The rats in the control group received daily intraperitoneal injections of saline, and those in STZ+H2S group and H2S group were given NaHS (100μmol/kg) injections. After 8 weeks, the pathologies of cardiac fibrosis were examined with HE staining, and the expressions of collagen I, MAPK1/3 and MMP-8 were analyzed with Western blotting. Results Compared with the control group, the diabetic rats showed increased collagen content and obvious interstitial fibrosis in the myocardial tissue with significantly increased expression levels of collagen I, MAPK1/3 and MMP-8 (P<0.05); all these changes were obviously reversed by treatment with H2S (P<0.05). Collagen I, MAPK1/3 and MMP-8 expression levels and the degree of myocardial fibrosis were comparable between H2S group and control group (P>0.05). Conclusion Hydrogen sulfide can attenuate cardiac fibrosis in diabetic rats, and the mechanism may involve the inhibition of MAPK1/3/MMP-8 signal pathway.